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Infection and Immunity, April 2002, p. 2151-2158, Vol. 70, No. 4
0019-9567/02/$04.00+0     DOI: 10.1128/IAI.70.4.2151-2158.2002
Copyright © 2002, American Society for Microbiology. All Rights Reserved.

Early Enhanced Th1 Response after Leishmania amazonensis Infection of C57BL/6 Interleukin-10-Deficient Mice Does Not Lead to Resolution of Infection

Douglas E. Jones,1* Mark R. Ackermann,1 Ulrike Wille,2 Christopher A. Hunter,2 and Phillip Scott2

Department of Veterinary Pathology, College of Veterinary Medicine, Iowa State University, Ames, Iowa 50011,1 Department of Pathobiology, School of Veterinary Medicine, University of Pennsylvania, Philadelphia, Pennsylvania 191042

Received 13 September 2001/ Returned for modification 1 November 2001/ Accepted 21 December 2001

C3H and C57BL/6 mice are resistant to Leishmania major but develop chronic lesions with persistent parasite loads when they are infected with Leishmania amazonensis. These lesions develop in the absence of interleukin-4 (IL-4), indicating that susceptibility to this parasite is not a result of development of a Th2 response. Expression of the cytokine IL-10 during infection could account for the lack of IL-12 expression and poor cell-mediated immunity towards the parasite. Therefore, we tested the hypothesis that IL-10 plays a central role in downmodulating the Th1 response after L. amazonensis infection. Infection of C57BL/6 IL-10-deficient mice indicated that in the absence of IL-10 there was early enhancement of a Th1 response, which was downregulated during the more chronic stage of infection. In addition, although there were 1- to 2-log reductions in the parasite loads within the lesions, the parasites continued to persist, and they were associated with chronic lesions whose size was similar to that of the control lesions. These experiments indicated that L. amazonensis resistance to killing in vivo is only partially dependent on expression of host IL-10. However, IL-10-deficient mice had an enhanced delayed-type hypersensitivity response during the chronic phase of infection, indicating that there were Th1 type effector cells in vivo at this late stage of infection. These results indicate that although IL-10 plays a role in limiting the Th1 response during the acute infection phase, other immunomodulatory factors are responsible for limiting the Th1 response during the chronic phase.

* Corresponding author. Mailing address: Department of Veterinary Pathology, College of Veterinary Medicine, Iowa State University, Ames, IA 50011-1250. Phone: (515) 294-4682. Fax: (515) 294-5423. E-mail: jonesdou{at}iastate.edu.

Editor: W. A. Petri, Jr.

Infection and Immunity, April 2002, p. 2151-2158, Vol. 70, No. 4
0019-9567/02/$04.00+0     DOI: 10.1128/IAI.70.4.2151-2158.2002
Copyright © 2002, American Society for Microbiology. All Rights Reserved.



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